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For improving the emergency capacities during road transportation accidents of dangerous goods, this paper divides the accident emergency procedure into four subsystems: accident information processing, personnel rescue and evacuation, vehicle evacuation, and rescue materials delivery. On this basis, the causal mechanism and the loop diagrams of the emergency process are established by using the System Dynamics Method and Vensim software. First, six factors including transportation distance, the degree of mechanical modernization, delay time of personnel control, delay time of traffic information release, command level coefficient, and delay time of department arrival are selected as parameters to test the model's sensitivity analysis. Then, the influences of the abovementioned factors on the observed value, such as the demand gap of on-site materials, number of people in safe area, number of vehicles in safe area, amount of disposal information, and the dynamic evolution behavior of the system, are analyzed. The results show that the transportation distance is shortened by half, and the time to fill the demand gap is reduced by 39%. The level of mechanical modernization is doubled, the peak inventory of materials in transit will increase by 9.2%, and the time to reach the peak will be shortened by 6.8%. If the delay time of personnel control is shortened by 480s, the number of people to be evacuated in accident area will be reduced by 56. The delay time of traffic information release is shortened by 480s, the number of vehicles to be evacuated is reduced by 74, and the time when the vehicle stops entering accident area is 1646s in advance. The command level coefficient increases by 9.5%, and the speed of action execution increases by 9.6%., Author(s): Guo-sheng Zhang [1]; Xiao-yan Shen (corresponding author) [2]; Jun Hua [3]; Jun-wei Zhao [3]; Hao-xue Liu [2] 1. Introduction Dangerous goods are an important support for the normal operation [...]

In this study, we investigated the effect of astragaloside IV on skeletal muscle energy metabolism disorder caused by statins and explored the possible mechanisms. High-fat diet-fed apolipoprotein E knockout (ApoE-/- ) mice performed aerobic exercise and were administered simvastatin, simvastatin + trimetazidine, or simvastatin + astragaloside IV by gavage. At the end of treatment, exercise performance was assessed by the hanging grid test, forelimb grip test, and running tolerance test. Moreover, plasma lipid and creatine kinase concentrations were measured. After sacrifice, the gastrocnemius muscle was used to assess muscle morphology, and energy metabolism was evaluated by determining the concentration of lactic acid and the storage capacity of adenosine triphosphate and glycogen. Mitochondrial function was assessed by measuring mitochondrial complex III and citrate synthase activity and membrane potential. In addition, oxidative stress was assessed by determining the level of hydrogen peroxide. Finally, using western blotting and reverse transcription polymerase chain reaction, we explored the mechanism of astragaloside IV in alleviating simvastatin-induced muscle injury. Our results demonstrated that astragaloside IV reversed simvastatin-induced muscle injury without affecting the lipid-lowering effect of simvastatin. Moreover, astragaloside IV promoted the phosphorylation of AMPK and activated PGC-1α, which upregulated the expression of NRF1 to enhance energy metabolism and inhibit skeletal muscle cell apoptosis. [ABSTRACT FROM AUTHOR]

Brain 'Computer Interface (BCI) is an emerging technology for communication between human brain and external devices. The traditional feature extraction method based on time-frequency characteristics cannot reflect the nonlinear characteristics of EEG signals. In order to further improve the accuracy of classification, the pretreatment method of wave threshold denossing is firstly used to improve the signal-to-noise ratio of EEG signals. Then, the feature extraction of the three kinds of imaginary motion EEG signal is carried out by the parameter-sample entropy of nonlinear dynamics, and the nonlinear features of EEG signal are preserved. Among them, the research of Motor-Imagery (MI) EEG has always been the focus of BCI that is a highspeed development field. This paper studies three classifiers including support vector machine, LVQ neural network and BP neural network. The experimental results show that BP neural network has higher recognition rate for classification and recognition of EEG signal. [ABSTRACT FROM AUTHOR]

As a special type of lung cancer, multiple primary lung cancer (MPLC) has unique biological characteristics, and its research remains limited. The aim of our research was to identify prognostic factors and construct a prognostic nomogram of dual primary lung cancer (DPLC). A population cohort study of patients with DPLC was conducted using the extracted data from the Surveillance, Epidemiology, and End Results (SEER) database. Relevant survival variables were identified using the Cox proportional hazard model. Prognostic nomogram was performed and its predictive performance was validated via the modeling and validating cohort data. Additionally, propensity score matching (PSM) was also applied to evaluate whether surgery affected the OS of this study population. 5411 eligible DPLC patients were included in this study cohort, with 41.0% of 3-year OS rate and 27.7% of 5-year OS rate. Age, sex, race, grade, stage, lymph node (LN) metastasis, histological type, primary site, and surgery were considered to be prognostic factors of OS. The C-indexes of the established nomogram were 0.70 (95% CI (0.69, 0.71)) in the modeling group and 0.70 (95% CI (0.68, 0.72)) in the validation group, which showed an ideal model discrimination ability. AUC and calibration plots of 3- and 5-year OS also proved the good performance of the established nomogram. After 1 : 1 PSM, surgery can potentially reduce the risk of OS (HR = 0.63, 95% CI: 0.56–0.72) of DPLC. The prognostic nomogram with reliable performance was developed to predict 3- and 5-year OS rates, which could assist clinicians to make more reasonable survival prediction for DPLC patients. For patients without absolute surgical contraindications, surgery should be actively considered. [ABSTRACT FROM AUTHOR]

To seek out novel promising biomarkers for predicting lung adenocarcinoma (LUAD) prognosis, we conducted this study. First, 279 upregulated and 37 downregulated differentially expressed genes were obtained from LUAD and para‐carcinoma tissues by the Affymetrix GeneChip Human Transcriptome Array. Then, we randomly classified samples of LUAD data set GSE31210 as training and testing sets in a 1:1 ratio. Alcohol dehydrogenase 1C (ADH1C) and secreted phosphoprotein 1 (SPP1) were finally identified correlating with the LUAD survival through least absolute shrinkage and selection operator penalized Cox proportion hazards regression model, and applied to build a 2‐gene signature related to prognosis in training set. Univariate and multivariable survival analyses suggested that overall survival (OS) and relapse‐free survival (RFS) in the 2‐gene signature low‐risk group were better than the high‐risk group. Kaplan–Meier curves proved that elevated ADH1C expression and reduced SPP1 expression were related to better OS and RFS. Besides, the SPP1 expressed higher in LUAD than para‐carcinoma tissues using quantitative reverse transcription polymerase chain reaction assay. Finally, the association between the two genes and clinicopathological parameters in 80 LUAD were analyzed, it is suggested that SPP1 was relevant to epidermal growth factor receptor mutation. These findings indicated that ADH1C and SPP1 might be novel promising biomarkers for predicting LUAD prognosis. [ABSTRACT FROM AUTHOR]

• Matrine improved the symptoms of CLP-induced sepsis mice. • Matrine reduced the levels of inflammatory factors in CLP-induced sepsis mice. • Matrine inhibited pyroptosis in THP-1 cells stimulated by nigericin or ATP. • Matrine suppressed NLRP3 inflammasome activation through regulating PTPN2/JNK/SREBP2 pathway. Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Abnormal activation of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome plays a vital role in the pathogenesis of sepsis. Matrine is proved to show good anti-inflammatory properties, whereas its effect and the underlying molecular machinery on sepsis remains unclear. The aim of this study is to evaluate the effect and mechanism of Matrine on sepsis. THP-1 cells and J774A.1 cells were stimulated by lipopolysaccharide (LPS) with nigericin or adenosine triphosphate (ATP) to establish an in vitro model. Cecal ligation and puncture (CLP)-induced sepsis mouse model was used. Matrine was given by gavage. To investigate the NLRP3 inflammasome activation, phorbol myristate acetate (PMA)-induced THP-1 cells were first primed with LPS and then stimulated by matrine, followed by treatment with nigericin or ATP. The concentration of interleukin 1β (IL-1β) and interleukin 18 (IL-18) in the cell culture supernatant was detected. The mechanism was explored by cell death assay, immunoblots and immunofluorescence in vitro. C57BL/6 mice were intragastrically administered with matrine for 5 days before CLP. The therapeutic effect of matrine was evaluated by symptoms, pathological analysis, ELISA and RT-qPCR. Our results revealed that matrine inhibited IL-1β and IL-18 secretion, suppressed caspase-1 activation, reduced cell death, and blocked ASC speck formation upon NLRP3 inflammasome activation. Furthermore, matrine restrains NLRP3 inflammasome activation as well as pyroptosis through regulating the protein tyrosine phosphatase non-receptor type 2 (PTPN2)/JNK/SREBP2 signaling. Matrine also prominently improved the symptoms and pathological changes with reduced levels of TNF-α, IL-1β, and IL-6 in the lung tissues and serum in a dose-dependent manner. Matrine effectively alleviates the symptoms of CLP-induced sepsis in mice, restrains NLRP3 inflammasome activation by regulating PTPN2/JNK/SREBP2 signaling pathway, and may become a promising therapeutic agent for sepsis treatment. [Display omitted] [ABSTRACT FROM AUTHOR]

The micro-electronic neural bridge (MENB) aims to rebuild lost motor function of paralyzed humans by routing movement-related signals from the brain, around the damage part in the spinal cord, to the external effectors. This study focused on the prototype system design of the MENB, including the principle of the MENB, the neural signal detecting circuit and the functional electrical stimulation (FES) circuit design, and the spike detecting and sorting algorithm. In this study, we developed a novel improved amplitude threshold spike detecting method based on variable forward difference threshold for both training and bridging phase. The discrete wavelet transform (DWT), a new level feature coefficient selection method based on Lilliefors test, and the k-means clustering method based on Mahalanobis distance were used for spike sorting. A real-time online spike detecting and sorting algorithm based on DWT and Euclidean distance was also implemented for the bridging phase. Tested by the data sets available at Caltech, in the training phase, the average sensitivity, specificity, and clustering accuracies are 99.43%, 97.83%, and 95.45%, respectively. Validated by the three-fold cross-validation method, the average sensitivity, specificity, and classification accuracy are 99.43%, 97.70%, and 96.46%, respectively. [ABSTRACT FROM PUBLISHER]

Background: Inflammatory bowel disease (IBD) is an autoimmune disease. The pathogenesis of IBD is complicated and intestinal mucosal barrier damage is considered as the trigger factor for the initiation and recurrence of IBD. Total Glucosides of Paeony (TGP) has shown good inhibitory effects on immune-inflammation in clinic studies. However, its effect and mechanism on IBD are largely unknown.Purpose: The purpose of this study is to evaluate the effect and mechanism of TGP on IBD.Study Design: DSS-induced colitis mouse model was used. TGP was given by gavage. Caco-2 cells were stimulated by outer membrane vesicles (OMV) to establish an in vitro model.Methods: C57BL/6 mice were divided into normal control group, model group, mesalazine group, paeoniflorin (PA) group, high-dose group of TGP, and low-dose group of TGP. The model was induced with 2.5% DSS for 7 days, and TGP was intragastrically administered for 10 days. The therapeutic effect of TGP was evaluated by symptoms, histochemical analysis, RT-qPCR and ELISA. The mechanism was explored by intestinal permeability, Western blot and immunofluorescence in vivo and in vitro.Results: Our results showed that TGP could significantly improve the symptoms and pathological changes, with reduced levels of TNF-α, IL-17A, IL-23 and IFN-γ in the colon tissues and serum under a dose-dependent manner. TGP also reduced the intestinal permeability and restored the protein expression of tight junction and adherens junction proteins of intestinal epithelial cells in vivo and in vitro. Furthermore, TGP could inhibit the expression of p-Lyn and Snail and prevent Snail nuclear localization, thereby maintaining tight and adherens junctions.Conclusion: TGP effectively improves the symptoms of DSS-induced colitis in mice, protects the intestinal epithelial barrier by inhibiting the Lyn/Snail signaling pathway, and maybe a promise therapeutic agent for IBD treatment. [ABSTRACT FROM AUTHOR]

Background: The development of rheumatoid arthritis (RA) is related to germinal center (GC) response and autoreactive T cells, which mediate adaptive immunity and play an important role in stimulating the production of autoantibodies and pro-inflammatory cytokines by B cells and macrophages. Total Glucosides of Paeony (TGP) has anti-inflammatory, immunomodulatory and analgesic effects and is widely used to treat RA. However, few studies investigated whether the therapeutic effect of TGP is associated with the inhibition of autoimmune response.Purpose: The aim of this study was to investigate the effects and mechanisms of TGP on RA.Study Design: Type II collagen-induced arthritis (CIA) mouse model was used, and TGP and paeoniflorin were intragastrically treated.Methods: DBA/1 mice were divided into 5 groups: control, model, positive drug (paeoniflorin) and high- and low-dose TGP group. After 21 days of intragastric administration, the pathological change, inflammation expression and molecular mechanism of each group of mice were detected by Micro-CT, histochemical analysis, ELLSA, Western blot, RT-qPCR and flow cytometry.Results: Our study found that TGP treatment effectively improved inflammation and joint destruction in CIA mice. It reduced the production of serum IgG2a and pro-inflammatory cytokines, including serum interleukin (IL)-21, tumor necrosis factor (TNF)-α and IL-6, and the phosphorylation of NF-κB p65 and STAT3 in a dose-dependent manner. More importantly, TGP could suppress the frequency of germinal center B cells and Tfh cells in the spleen.Conclusion: TGP can not only improve symptoms, but also inhibit bone destruction. The therapeutic effect of TGP on CIA is mainly achieved by inhibiting spleen Tfh cell differentiation and GC formation through STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Ethnopharmacological relevance Jiang-Xian HuGan (JXHG) formulated by five natural products including Freshwater clam (Corbicula fluminea) , Curcuma longa L., Ligustrum lucidum , Eclipta prostrata (L.) L. and Paeonia lactiflora Pall. , has exhibited a great hepatoprotective effect. Aim of this study We investigated the effect of JXHG on concanavalin A (ConA)-induced acute live injury in mice, and to elucidate its underlying molecular mechanisms. Materials and methods Jiangkanling Capsule (900 mg/kg), low-dose JXHG (LJXHG, 700 mg/kg), high-dose JXHG (HJXHG, 1400 mg/kg) were administered to mice by oral gavage daily for 20 days prior to a single intravenous injection of ConA (20 mg/kg). Liver injury was evaluated by measuring the serum levels of enzymes and cytokines as well as liver histological analysis. We also measured the hepatic expression of cytokines at mRNA levels and the proteins related to NF-κB and Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling pathways. Result Our results showed that JXHG pretreatment significantly alleviated ConA-induced live injury as evidenced by decreased serum levels of glutamic-pyruvic transaminase (ALT) and glutamic oxalacetic transaminase (AST), and reduced hepatocyte apoptosis and mortality. Furthermore, JXHG was able to significantly reduce the serum levels of proinflammatory cytokines, down-regulate the mRNA expression of interleukin-6 (IL-6) and interferon-γ (IFN-γ), and up-regulate IL-10 as well as superoxide-dimutase-1 (SOD1), glutathione reductase (GSR) and Glutathione peroxidase 2 (GPX2) mRNA in the liver tissues after Con A injection. In addition, JXHG pretreatment dramatically suppressed the phosphorylation of NF-κB p65 (p65), increased Nrf2 expression, and decreased the expression ratio of cleaved caspase-3/caspase-3 in liver tissues. Conclusion These results suggest that JXHG protects against ConA-induced acute live injury through inhibiting NF-κB mediated inflammatory pathway and promoting Nrf2 mediated anti-oxidative stress signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Speech disorders have a substantial impact on communication abilities and quality of life. Traditional treatments such as speech and psychological therapies frequently demonstrate limited effectiveness and patient compliance. Transcranial electrical stimulation (TES) has emerged as a promising non-invasive treatment to improve neurological functions. However, its effectiveness in enhancing language functions and serum neurofactor levels in individuals with speech disorders requires further investigation., Aim: To investigate the impact of TES in conjunction with standard therapies on serum neurotrophic factor levels and language function in patients with speech disorders., Methods: In a controlled study spanning from March 2019 to November 2021, 81 patients with speech disorders were divided into a control group ( n = 40) receiving standard speech stimulation and psychological intervention, and an observation group ( n = 41) receiving additional TES. The study assessed serum levels of ciliary neurotrophic factor (CNTF), glial cell-derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), and nerve growth factor (NGF), as well as evaluations of motor function, language function, and development quotient scores., Results: After 3 wk of intervention, the observation group exhibited significantly higher serum levels of CNTF, GDNF, BDNF, and NGF compared to the control group. Moreover, improvements were noted in motor function, cognitive function, language skills, physical abilities, and overall development quotient scores. It is worth mentioning that the observation group also displayed superior performance in language-specific tasks such as writing, reading comprehension, retelling, and fluency., Conclusion: This retrospective study concluded that TES combined with traditional speech and psychotherapy can effectively increase the levels of neurokines in the blood and enhance language function in patients with speech disorders. These results provide a promising avenue for integrating TES into standard treatment methods for speech disorders., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Mild cognitive impairment(MCI)has a high risk of progressing to dementia,with no recommended therapies.Recent studies have shown that meditation has huge potential to improve the cognitive function,with low cost and high safety,being suitable to be applied in the treatment of neurological and psychotic disorders.This paper reviews the application and prospects of meditation in treating MCI from the concept,clinical efficacy,and mechanism of meditation,aiming to provide reference for future clinical studies.

Functional electrical stimulation is an effective way to rebuild hindlimb motor function after spinal cord injury. However, no site map exists to serve as a reference for implanting stimulator electrodes. In this study, rat models of thoracic spinal nerve 9 contusion were established by a heavy-impact method and rat models of T6/8/9 spinal cord injury were established by a transection method. Intraspinal microstimulation was performed to record motion types, site coordinates, and threshold currents induced by stimulation. After transection (complete injury), the core region of hip flexion migrated from the T13 to T12 vertebral segment, and the core region of hip extension migrated from the L1 to T13 vertebral segment. Migration was affected by post-transection time, but not transection segment. Moreover, the longer the post-transection time, the longer the distance of migration. This study provides a reference for spinal electrode implantation after spinal cord injury. This study was approved by the Institutional Animal Care and Use Committee of Nantong University, China (approval No. 20190225-008) on February 26, 2019., Competing Interests: None

Aim: To ensure the diagnostic value of computer aided techniques in diabetic retinopathy (DR) detection based on ophthalmic photography (OP)., Methods: PubMed, EMBASE, Ei village, IEEE Xplore and Cochrane Library database were searched systematically for literatures about computer aided detection (CAD) in DR detection. The methodological quality of included studies was appraised by the Quality Assessment Tool for Diagnostic Accuracy Studies (QUADAS-2). Meta-DiSc was utilized and a random effects model was plotted to summarize data from those included studies. Summary receiver operating characteristic curves were selected to estimate the overall test performance. Subgroup analysis was used to identify the efficiency of CAD in detecting DR, exudates (EXs), microaneurysms (MAs) as well as hemorrhages (HMs), and neovascularizations (NVs). Publication bias was analyzed using STATA., Results: Fourteen articles were finally included in this Meta-analysis after literature review. Pooled sensitivity and specificity were 90% (95%CI, 85%-94%) and 90% (95%CI, 80%-96%) respectively for CAD in DR detection. With regard to CAD in EXs detecting, pooled sensitivity, specificity were 89% (95%CI, 88%-90%) and 99% (95%CI, 99%-99%) respectively. In aspect of MAs and HMs detection, pooled sensitivity and specificity of CAD were 42% (95%CI, 41%-44%) and 93% (95%CI, 93%-93%) respectively. Besides, pooled sensitivity and specificity were 94% (95%CI, 89%-97%) and 87% (95%CI, 83%-90%) respectively for CAD in NVs detection. No potential publication bias was observed., Conclusion: CAD demonstrates overall high diagnostic accuracy for detecting DR and pathological lesions based on OP. Further prospective clinical trials are needed to prove such effect., (International Journal of Ophthalmology Press.)

Oxidative stress and neuroinflammation are important in the pathogenesis of ageing and age‑related neurodegenerative diseases, including Alzheimer's disease. NADPH oxidase 2 (NOX2) is a major source of reactive oxygen species (ROS) in the brain. The nucleotide‑binding oligomerisation domain (NOD)‑like receptor protein 1 (NLRP1) inflammasome is responsible for the formation of pro‑inflammatory molecules in neurons. Whether the NOX2‑NLRP1 inflammasome signalling pathway is involved in neuronal ageing and age‑related damage remains to be elucidated. Ginsenoside Rg1 (Rg1) is a steroidal saponin found in ginseng. In the present study, the primary hippocampal neurons were treated with H2O2 (200 µM) and Rg1 (1, 5 and 10 µM) for 24 h to investigate the protective effects and mechanisms of Rg1 on H2O2‑induced hippocampal neuron damage, which mimics age‑related damage. The results showed that H2O2 treatment significantly increased ROS production and upregulated the expression of NOX2 and the NLRP1 inflammasome, and led to neuronal senescence and damage to hippocampal neurons. Rg1 decreased ROS production, reducing the expression of NOX2 and the NLRP1 inflammasome in H2O2‑treated hippocampal neurons. Furthermore, Rg1 and tempol treatment significantly decreased neuronal apoptosis and the expression of β‑galactosidase, and alleviated the neuronal senescence and damage induced by H2O2. The present study indicates that Rg1 may reduce NOX2‑mediated ROS generation, inhibit NLRP1 inflammasome activation, and inhibit neuronal senescence and damage.

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disorder. Hydrogen sulfide (H 2 S), the third physiological gasotransmitter, is well recognized as an anti-inflammatory mediator in various inflammatory conditions. Herein, we explored the protective effects of S-propargyl-cysteine (SPRC, also known as ZYZ-802), an endogenous H 2 S modulator, on RA and determined the underlying mechanisms. In the present study, SPRC concentration-dependently attenuated inflammatory mediator expression, reactive oxidase species generation, and the expression and activity of matrix metalloproteinases (MMP)-9 in interleukin (IL)-1β-induced human rheumatoid fibroblast-like synoviocytes MH7A. In addition, SPRC blocked IL-1β-mediated migration and invasion of MH7A cells. As expected, the protective effects of SPRC were partially abrogated by DL-propargylglycine (PAG, a H 2 S biosynthesis inhibitor). In vivo study also demonstrated that SPRC treatment markedly ameliorated the severity of RA in adjuvant-induced arthritis rats, and this effect was associated with the inhibition of inflammatory response. We further identified that SPRC remarkably induced heme oxygenase-1 expression associated with the degradation of Kelch-like ECH-associated protein 1 (Keap1) and nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2); this effect was attributed to the sulfhydrylation of the cysteine residue of Keap1. Our data demonstrated for the first time that SPRC, an endogenous H 2 S modulator, exerted anti-inflammatory properties in RA by upregulating the Nrf2-antioxidant response element (ARE) signaling pathway., (Copyright © 2016. Published by Elsevier B.V.)

Rebuilding the damaged motor function caused by spinal cord injury is one of the most serious challenges in clinical neuroscience. The function of the neural pathway under the damaged sites can be rebuilt using functional electrical stimulation technology. In this study, the locations of motor function sites in the lumbosacral spinal cord were determined with functional electrical stimulation technology. A three-dimensional map of the lumbosacral spinal cord comprising the relationship between the motor function sites and the corresponding muscle was drawn. Based on the individual experimental parameters and normalized coordinates of the motor function sites, the motor function sites that control a certain muscle were calculated. Phasing pulse sequences were delivered to the determined motor function sites in the spinal cord and hip extension, hip flexion, ankle plantarflexion, and ankle dorsiflexion movements were successfully achieved. The results show that the map of the spinal cord motor function sites was valid. This map can provide guidance for the selection of electrical stimulation sites during the rebuilding of motor function after spinal cord injury., Competing Interests: Conflicts of Interest: None declared.